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  Table of Contents    
ORIGINAL ARTICLE  
Year : 2023  |  Volume : 25  |  Issue : 116  |  Page : 1-7
Middle Ear Muscle Reflex in Normal-Hearing Individuals with Occupational Noise Exposure

1 Facility for Advanced Auditory Research (FAAR), Department of Audiology, All India Institute of Speech and Hearing, Mysuru, Karnataka, India
2 Department of Audiology, All India Institute of Speech and Hearing, Mysuru, Karnataka, India

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Date of Submission17-Jan-2022
Date of Acceptance27-Jun-2022
Date of Web Publication27-Mar-2023
 
  Abstract 


Objectives: Noise-induced cochlear synaptopathy is studied extensively in animal models. The diagnosis of synaptopathy in humans is challenging and the roles of many noninvasive measures in identifying synaptopathy are being explored. The acoustic middle ear muscle reflex (MEMR) can be considered as a vital tool since noise exposure affects the low-spontaneous rate fibers that play an important role in elicitation of MEMR. The present study aimed at measuring MEMR threshold and MEMR strength. Design: The study participants were divided into two groups. All the participants had normal-hearing thresholds. The control group consisted of 25 individuals with no occupational noise exposure whereas noise exposure group had 25 individuals who were exposed to occupational noise of 85 dBA for a minimum period of 1 year. MEMR threshold and strength was assessed for pure tones (500 Hz and 1000 Hz) and broadband noise. Results: The results showed that the MEMR threshold was similar in both the groups. MEMR strength was reduced in noise exposure group compared to control group. Conclusions: The results of the study suggest that MEMR strength could be used as a sensitive measure in identifying cochlear synaptopathy with careful consideration of the stimulus characteristics.

Keywords: Acoustic reflex, cochlear neuropathy, cochlear synaptopathy, hidden hearing loss, middle ear muscle reflex

How to cite this article:
Vasudevamurthy S, Kumar AU. Middle Ear Muscle Reflex in Normal-Hearing Individuals with Occupational Noise Exposure. Noise Health 2023;25:1-7

How to cite this URL:
Vasudevamurthy S, Kumar AU. Middle Ear Muscle Reflex in Normal-Hearing Individuals with Occupational Noise Exposure. Noise Health [serial online] 2023 [cited 2023 Sep 27];25:1-7. Available from: https://www.noiseandhealth.org/text.asp?2023/25/116/1/372593



  Introduction Top


Noise exposure over a prolonged period is hazardous to the auditory system. Acoustic overexposure results in damage to the sensory cells, synapses between hair cells and the auditory nerve, spiral ganglion cells, and the auditory nerve. Depending on the extent of damage caused to the structures, a temporary or permanent threshold shift is seen. Recent evidence suggests that though the acute damage to the hair cell and resulting elevation hearing thresholds are reversible, damage to spiral ganglion cells, synapse, and the nerves are not.[1] Liberman et al. [2]showed that acoustic overexposure resulted in acute loss of synapses between auditory nerve and inner hair cells. This was followed by slow onset neural degeneration. Furthermore, the low-spontaneous rate, high-threshold auditory nerve fibers are more vulnerable to noise exposure than high-spontaneous rate, low-threshold fibers.[3] This permanent loss of auditory nerve synapses was seen despite a recovery in absolute sensitivity and cochlear function. It is hypothesized that permanent damage of auditory nerve synapses might lead to deficits in hearing in noise and suprathreshold auditory processing skills, even when the hearing thresholds are normal. This type of hearing impairment is termed cochlear synaptopathy[1] or hidden hearing loss.[4]

Histopathological investigations in animals exposed to loud noise have confirmed the presence of cochlear synaptopathy.[5],[6],[7],[8],[9] Previous animal work also has revealed reduced amplitude of compound action potential at suprathreshold intensities along with normal otoacoustic emissions (OAEs) and hearing thresholds as the hallmark of cochlear synaptopathy in animals.[5],[8],[10],[11] In addition, animal studies have shown a good relationship between synapse/auditory nerve (AN) loss and suprathreshold amplitude of wave I.[5],[6],[7] However, as invasive studies are not feasible, human studies are indecisive about the presence of cochlear synaptopathy. Many electrophysiological (auditory brainstem response (ABR), electrocochleography, and envelope following response (EFR)) and behavioral tests (such as high-frequency audiometry and speech perception in noise) are used as proxy measures to observe cochlear synaptopathy in humans.[12] In a systematic review, Barbee et al.[12] concluded that suprathreshold wave I amplitude and the summating potential (SP)/action potential (AP) ratio of electrocochleography (ECochG) are promising tools in identifying individuals at risk for cochlear synaptopathy or hidden hearing loss in humans. However, Plack et al.[13] report high intersubject variability for wave I amplitude of ABR. Also, other electrophysiological measures like EFR fail to provide consistent evidence for cochlear synaptopathy in humans.[14]

Recent studies of cochlear synaptopathy have considered the use of middle ear muscle reflex (MEMR) as a diagnostic tool. It is believed that the MEMR pathway involves low-spontaneous rate and high-thresholds afferent neurons.[15],[16] As animal models have shown that noise exposure causes selective damage to the high-threshold, low-spontaneous rate fibers , it was assumed that the MEMR might be sensitive in diagnosing cochlear synaptopathy. In mice, MEMR was found to be an indicator of cochlear synaptopathy.[17] Valero et al.[18] also report that the MEMR outperformed suprathreshold ABR wave I amplitude in indicating cochlear synaptopathy in animals. Wojtczak et al.[19] found reduced MEMR strength in normal-hearing individuals with tinnitus. In humans, a few studies have explored the relationship between MEMR and other potential correlates of synaptopathy, such as speech perception in noise and lifetime noise exposure. However, results of these studies are inconclusive. Some studies have reported a significant correlation between the MEMR and speech perception in noise, Mepani et al. and Shehorn et al.[20],[21] while others failed to show such relationship Guest et al.[22] Also, Causon et al.[23] failed to show any relationship between lifetime noise exposure and MEMR. Importantly, all these studies used interviews, self-reports, or questionnaires to estimate the noise exposure. It is plausible that retrospective self-report may not reliably capture the noise exposure. Since, MEMR involves low-spontaneous rate fibers, and can be measured quickly with good test-retest reliability,[24],[25] more research is required before it can be used as a diagnostic tool for identifying cochlear synaptopathy. Thus, this study intended to compare the MEMR threshold and MEMR strength in a group of individuals exposed to high levels of occupational noise.


  Materials and methods Top


The study used static group comparison research design. All the participants were informed about the aims and objectives of the study. Participation in the study was voluntary and all participants signed an informed consent form. The ethical guidelines for Bio-behavioral Research at All India Institute of Speech and Hearing, Mysore was followed and the ethical board of All India Institute of Speech and Hearing approved the study.[26]

Participants

A total of 50 male participants were recruited for the study. All participants were native listeners of Kannada, a South Indian language. Based on the exposure to occupation noise, they were divided into either noise exposure group (20–26 years; mean age: 22.4 years) or the control group (20–27 years: mean age: 21.4 years) with 25 participants in each group. The individuals in the control group were screened using a noise exposure questionnaire and they had no exposure to loud domestic noise or occupational noise.[27] Participants in the noise exposure group were exposed to industrial noise on an average of 3.6 years. They worked in a heavy machinery manufacturing industry. All workers worked 8-hour shifts. Through structured interview, it was found that the workers did not use hearing protection devices regularly. Noise survey carried out in the industry showed that the workplace’s noise level was 85 dBA. The noise measurements were carried out with a calibrated sound level meter (Bruel and Kjaer 2270, Naerem, Denmark) as per Bureau of Indian Standards (BIS) standards (IS: 7194; 1994).[28] Eighty-five dBA represents the average noise levels during working hours in the places where participants worked. Pure-tone hearing thresholds were within 25 dB SPL in all participants. Independent samples t test showed that the air conduction pure-tone thresholds (at octave frequencies from 250 Hz–8 kHz) did not differ significantly between the groups in both right and left ear. [Table 1] shows the test statistic and significance for all the frequencies in both right and left ear. Transient-evoked otoacoustic emission (TEOAE) global amplitude was >6 dB in all the participants. Also, TEOAE signal to noise ratio was >6 dB for three consecutive frequencies between 1000 Hz and 4000 Hz in all participants. Independent samples t test showed no significant differences in the TEOAE global amplitudes between two groups in both right (t = −1.453; P = 0.153) and left ear (t = −1.666: P = 0.102). [Figure 1]a and b show the mean and one standard deviation of pure-tone hearing thresholds and TEOAE amplitudes in noise exposure and control groups, respectively. All the participants had “A” type tympanogram with normal ipsilateral and contralateral acoustic reflexes at normal levels for 500 Hz, 1000 Hz, and 2000 Hz. A structured interview ensured that none of the participants had any otological or neurological problems. Mini-mental state examination was administered to rule out any cognitive issues.[29]
Table 1 Independent t test for pure-tone hearing thresholds across frequencies in both right and left ear

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Figure 1 (a) Mean and one standard deviation of the pure-tone hearing thresholds of both right and left ear in the control group and noise exposure group. (b) Mean and one standard deviation of the transient-evoked otoacoustic emissions (TEOAE) amplitudes of both right and left ear in control group and noise exposure group. The filled dots and the stars indicate the mean in the control group and noise exposure group, respectively. The error bars represent the one standard deviation from the mean.

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Procedure

The MEMR threshold and strength was assessed using the Titan with IMP440 impedance system (Interacoustics, Denmark).

Procedure for MEMR threshold

The MEMR threshold was assessed using three elicitors − 500 Hz, 1000 Hz, and broadband noise (BBN), presented contralaterally. A probe with a suitable ear tip was placed in the other ear, and a hermetic seal was achieved. Static admittance at the tympanometric peak pressure was monitored in the nontest using a 226 Hz probe signal. For all three elicitors, the initial presentation level was 80 dB HL, and the intensity was increased further in 5 dB steps. The lowest intensity that caused a reduction in middle ear admittance of >0.03 mL was considered as the MEMR threshold.

Procedure for MEMR strength

MEMR strength was measured in the same session as that of MEMR thresholds, and used the same elicitors as that of MEMR threshold. The MEMR strength was assessed by measuring absolute amplitudes of MEMR across different intensities and by calculating the slope of the MEMR growth function. The initial presentation level was 80 dB HL for all the elicitors. The maximum presentation level was 110 dB HL for 500 Hz, 115 dB HL for 1000 Hz, and 120 dB HL for BBN or uncomfortable level of the participant, whichever was lower. The amplitudes at different intensities were compared between the groups to assess the MEMR strength. The slope of the amplitude growth function was obtained for each participant and this measure was used for further analysis.


  Results Top


The data were analyzed using Statistical Package for the Social Sciences software (version 20, IBM, New York, USA). Greenhouse–Geisser correction was considered wherever the data violated the assumptions of sphericity.

MEMR threshold

[Figure 2] shows the mean, one standard deviation, and individual participants’ MEMR threshold across all the elicitors in both the groups. Two-way mixed analysis of variance (ANOVA) was performed with elicitors and ear as within-subject and group as between-subject factors. The results of the mixed ANOVA revealed a significant main effect of elicitor (F(2,96) = 27.150; P = 0.000; η2p = 0.361) but not group (F(1,48) = 2.424; P = 0.126; η2p = 0.048) and ear (F(1,49) = 0.029; P = 0.867; η2p = 0.001). Also, there was no significant interaction between the elicitor and group (F(2,96) = 0.249; P = 0.771; η2p = 0.005). As no main effect of ear was observed, the data of both the ears were combined (averaged) for further analysis. Separate one-way repeated measures ANOVA (RM-ANOVAs) were performed to check the effect of elicitor within each group. The results showed a significant main effect of elicitor in both the control (F(2,48) = 17.558; P = 0.000; η2p = 0.423) and the noise exposure group (F(2,48) = 10.783; P = 0.000; η2p = 0.310). Further, post hoc pairwise comparison indicated that the acoustic reflex threshold (ART) for BBN was significantly <500 Hz and 1000 Hz in both groups.
Figure 2 Mean and one standard deviations of the middle ear muscle reflex (MEMR) threshold across all the elicitors in both the groups. The filled dots and the stars represent the individual data points in the control group and noise exposure group, respectively. The error bars represent one standard deviation from the mean.

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MEMR strength

The MEMR strength was analyzed in terms of MEMR amplitudes and the slope of MEMR growth function. [Figure 3] shows the mean, standard deviation, and individual data points of MEMR amplitudes across different intensities for all the elicitors in both the groups. The statistical analysis was performed separately for each of the elicitors as the intensity levels varied among the three elicitors.
Figure 3 (a) Mean and one standard deviation of the MEMR amplitudes across different intensities for 500 Hz in both the groups. (b) Mean and one standard deviation of the MEMR amplitudes across different intensities for 1000 Hz in both the groups. (c) Mean and one standard deviation of the MEMR amplitudes across different intensities for broadband noise (BBN) in both the groups. The filled dots and the stars represent the individual data points in the control group and noise exposure group, respectively. The error bars represent one standard deviation from the mean.

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MEMR amplitudes for 500 Hz

Two-way mixed ANOVA was performed with the intensity and ear as within-subject and group as between-subject factors. The results showed a significant main effect of intensity (F(6,288) = 469.849; P = 0.000; η2p = 0.907) and group (F(1,48) = 15.939; P = 0.000; η2p = 0.249), and a significant interaction between intensity and group (F(6,288) = 0.003; P = 0.000; η2p = 0.230). Since no main effect of ear (F(1,48) = 0.318; P = 0.575; η2p = 0.007) was observed, the data of both the ears were combined for further analysis. A separate one-way RM-ANOVA was performed in both the groups to see the effect of intensity. The result showed a significant main effect of intensity in both the control (F(6,144) = 221.077; P = 0.000; η2p = 0.902) and the noise exposure group (F(6,144) = 297.304; P = 0.000; η2p = 0.925). Further post hoc pairwise comparisons revealed that the MEMR amplitude significantly increased through 80 dB HL to 110 dB HL in both the groups. Independent t test with alpha correction for multiple comparisons (new alpha value, P = 0.05/7 = 0.0071) was performed to see the difference in amplitude across intensities between the groups. The results showed that the MEMR amplitude was significantly higher in the control group than noise exposure group for intensities >90 dB HL. [Table 2] shows the test statistic and significance values for all the intensities. The observed effects were large for 90 dB HL and very large for all higher intensities.
Table 2 Independent t test for MEMR amplitudes for all the intensities across the three elicitors

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MEMR amplitudes for 1000 Hz

Two-way mixed ANOVA was performed similar to 500 Hz. The results showed a significant main effect of intensity (F(7,336) = 382.971; P = 0.000; η2p = 0.889) and group (F(1,48) = 15.780; P = 0.000; η2p = 0.259), and a significant interaction between intensity and group (F(7,336) = 16.092; P = 0.000; η2p = 0.251). Main effect of ear was not significant (F(1,48) = 0.288; P = 0.594; η2p = 0.006) and hence, the data of both the ears were combined for further analysis. A separate one-way RM-ANOVA was performed in both the groups to see the effect of intensity. The result showed a significant main effect of intensity in both the control (F(7,168) = 212.743; P = 0.000; η2p = 0.899) and the noise exposure group (F(7,168) = 80.125; P = 0.000; η2p = 0.770). Further post hoc pairwise comparisons revealed that the MEMR amplitude significantly increased through 80 dB HL to 115 dB HL in both the groups. Independent t test with alpha correction for multiple comparisons (new alpha value, P = 0.05/8 = 0.00625) was performed to see the difference in amplitude across intensities between the groups. The results showed that the MEMR amplitude was significantly higher in the control group than noise exposure group for all the intensities >90 dB HL except 95 dB HL. The test statistic and significance values are shown in [Table 2]. The observed effects were large for 90 dB HL and very large for intensities >100 dB HL.

MEMR amplitudes for BBN

Results of two-way mixed ANOVA showed a significant main effect of intensity (F(8,384) = 537.420; P = 0.000; η2p = 0.918) and group (F(1,48) = 18.000, P = 0.000, η2p = 0.273), and a significant interaction between intensity and group (F(8,384) = 12.572; P = 0.000; η2p = 0.208). Main effect of ear was not present (F(1,48) = 1.362; P = 0.249; η2p = 0.028) and hence, the data of both the ears were combined for further analysis. A separate one-way RM-ANOVA was performed in both the groups to see the effect of intensity. The result showed a significant main effect of intensity in both the control (F(8,192) = 236.617; P = 0.000; η2p = 0.908) and the noise exposure group (F(8,192) = 384.606; P = 0.000; η2p = 0.949). Further post hoc pairwise comparisons revealed that the MEMR amplitude significantly increased through 80 dB HL to 120 dB HL in both the groups. Independent t test with alpha correction for multiple comparisons (new alpha value, P = 0.05/9 = 0.0055) was performed to see the difference in amplitude across intensities between the groups. The results showed that the MEMR amplitude was significantly higher in the control group than noise exposure group for all the intensities >90 dB HL (see [Table 2] for test statistic and significance values). The observed effects were large for 90 dB HL and very large for higher intensities.

MEMR slope

The slope was calculated by fitting a linear regression between the MEMR amplitude and reflex elicitor level in dB SL (with respect to MEMR threshold).[23],[30],[31] This slope represents the rate of change of MEMR amplitude per dB increase in elicitor level. The slope was calculated individually for all the participants across three elicitors. [Figure 4] shows the mean and standard deviations of the slope of MEMR growth for all the elicitors in both groups. Two-way mixed ANOVA was performed with the elicitors and ear as within-subject factor and group as between-subject factor. The results showed a significant main effect of elicitor (F(2,96) = 25.884; P = 0.000; η2p = 0.350) and group (F(1,48) = 28.921; P = 0.000; η2p = 0.376). No significant interaction between elicitor and group (F(2,96) = 2.258; P = 0.110; η2p = 0.045) was seen. Main effect of ear was not significant (F(1,48) = 0.587; P = 0.447; η2p = 0.012) and hence, the data of both the ears were combined for further analysis. One-way RM-ANOVA was performed separately in each of the groups to see the effect of elicitor. The results indicated a significant main effect of elicitor only in the control group (F(2,48) = 11.937; P = 0.000; η2p = 0.332). Noise exposure group failed to show a significant main effect of elicitor (F(2,48) = 2.297; P = 0.114; η2p = 0.087). Further post hoc pairwise comparison revealed that in control group, the slope of MEMR growth was significantly shallower for 500 Hz than 1000 Hz and BBN. Since there was a significant main effect of group, independent sample t test was performed to see the differences between the groups for each of the elicitors. The results revealed a significant difference between the groups for 1000 Hz (t = 4.659; P = 0.000; d = 1.318) and BBN (t = 2.924; P = 0.005; d = 0.827). The slope was shallower in the noise exposure group for both 1000 Hz and BBN. There was no significant difference between two groups for 500 Hz (t = 1.270; P = 0.210; d = 0.357).
Figure 4 Mean and one standard deviations of the slope of MEMR growth for all the elicitors in both the groups. The filled dots and the stars represent the individual data points in the control group and noise exposure group, respectively. The error bars represent one standard deviation from the mean.

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  Discussion Top


The present study intended to measure the effect of occupational noise exposure on MEMR threshold and strength. Individuals exposed to occupational noise exhibited significantly reduced MEMR amplitude (for all the elicitors), and shallower MEMR slope (for 1000 Hz and BBN) compared to individuals not exposed to noise. However, MEMR threshold was found to be similar in both groups.

Wojtczak et al.[19] and Shehorn et al.[21] reported reduced MEMR strength in individuals with suspected cochlear synaptopathy. Wojtczak et al.[19] reported weaker MEMR in individuals with noise induced tinnitus. Shehorn et al.[21] reported significantly reduced MEMR amplitudes in a group of individuals who had sought help for self-reported hearing difficulties compared to the control group. Furthermore, they also reported a strong correlation between lifetime noise exposure, speech recognition performance, and MEMR strength. Reduced MEMR strength in these individuals could be attributed to differential damage of low-spontaneous rate fibers due to noise exposure.[19],[20] Low-spontaneous rate/high-threshold fibers are known to play a crucial role in eliciting MEMR.[15],[16] In combination with the above cited studies, our results provide strong evidence for MEMR magnitude as one of the sensitive measures for detecting cochlear synaptopathy.However, using similar stimuli and slope calculation procedure as in the present study, Causon et al.[23] found that noise exposure and MEMR growth were not related. It is important to note that previous studies on MEMR used presence of tinnitus or lifetime noise exposure to differentiate the group. However, the present study involved participants with documented exposure to occupational noise.


  Conclusions Top


The present study aimed at measuring MEMR threshold and strength in normal-hearing individuals exposed to occupational noise. It was found that the MEMR strength and slope was affected in the noise exposure group. However, MEMR threshold was not affected. In addition, it is important to consider the stimulus characteristics and the measurement procedure while comparing studies, as the results vary depending on the same. Future studies could consider the effect of different stimulus characteristics on MEMR growth in normal-hearing individuals with noise exposure.

Acknowledgements

Authors thank the Director, All India Institute of Speech and Hearing, Mysuru for permitting to conduct the study at the institute. Authors also thank the University of Mysuru.

Financial support and sponsorship

Authors thank DST for their support (Grant No. SR/CSRI/2017/61).

Conflicts of interest

There are no conflicts of interest



 
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Correspondence Address:
Sahana Vasudevamurthy
All India Institute of Speech and Hearing, Mysuru, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/nah.nah_3_22

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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1], [Table 2]



 

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